CSR Limited v Amaca Pty Ltd [2016] VSCA 320

CSR Limited v Amaca Pty Ltd [2016] VSCA 320 - VSCA 2016 case summary — Zoe

[140]

a. trade

Some trades were more likely to bring a worker into contact with asbestos than others. Obviously, a 'lagger' - a worker whose role it was to install or remove insulation around pipes and in boilers - was most likely to be exposed to airborne asbestos fibres. Depending on the type of insulation product being handled, the process of either installing or removing insulation could liberate a higher or lower amount of fibre. If, for example, KLite blocks were being installed on pipes with bends and angles or obstacles to negotiate, the calcium silicate blocks had to be cut at an angle for fitting purposes. Cutting was done with handsaws or mechanical saws. That process created a lot of dust which contained a percentage of amosite asbestos fibre.

A different trade - say, an instrument maker or a trade assistant to an instrument maker - may only have intermittently encountered an atmosphere with asbestos fibre, if at all, depending on whether asbestos insulation needed to be removed in order for an instrument to be installed or removed. It would also depend on whether that instrument maker was present when or soon after the asbestos insulation was disturbed.

Similarly, a cleaner or a rigger might be heavily exposed to asbestos fibre if working in an environment where insulation (say blocks or sections) had been cut leaving debris that could still be disturbed - even, in some cases, drifting down onto workers below. Or they may only be intermittently or rarely exposed to asbestos fibre if not working in and around insulation installation or removal areas or in periods of time when asbestos insulation product was not being disturbed.

But, the incidence of exposure for many of the trades working amongst those who worked more directly with asbestos fibre would be difficult to predict. It could readily be said that they might on occasions have been exposed to asbestos fibre: not that they must have been or, at least, not regularly.

The most comprehensive resource for information about a particular trade, and the nature and likely degree of exposure to airborne asbestos fibre associated with that trade, was supplied through Mr Drewett's OEAs for each claimant. As described in further detail below, Mr Drewett's statement, incorporating his OEAs, was permitted to be tendered subject to relatively few objections.

b. direct or indirect exposure

The degree of likelihood that a person's asbestos disease can be attributed to Hardie-BI asbestos, as distinct from other manufacturer's product, may be influenced by whether inferred exposure to Hardie-BI product was direct or indirect.

As previously explained, direct exposure is the inhalation of asbestos fibre in the industrial environment where the asbestos insulation is situated. Indirect exposure occurs through a worker, who him or herself being directly exposed, carries the asbestos fibre on clothing, boots etc into the home thus causing household members to come into contact with the dust which they inhale.

Common sense would suggest that the quantity fibre to which a household member may be indirectly exposed will generally be less than that of the directly exposed worker. But the extent of a household member's potential exposure will itself be impacted by the number of workers in the household who worked at an SECV facility; the trades that those workers worked in; the places each different worker worked in; the duration of time over which the workers carried the dust into the home; the particular tasks the household member had with the clothing; and the extent to which the person's asbestos condition can be sensibly explained by exposure to any other source, and so on.

c. period

Where the supply and construction records for the particular facility indicated the probable installation of Hardie-BI product from a specific point in time, it is obviously relevant to know whether the claimant was present at the facility thereafter, or only before. It is also relevant to know the duration of a claimant's work at a particular facility at which Hardie-BI fibre can be inferred to have been installed. Clearly, the longer a claimant worked at a facility, the higher the degree of probability that he or she encountered airborne asbestos fibre liberated from Hardie-BI product.

But it is also highly relevant to know whether the period of the worker's presence at a facility was during a construction phase or only a maintenance phase. It stands to reason that the disturbance of asbestos fibre into the atmosphere was likely to have occurred in greater volume when insulation was being installed in bulk, rather than removed and replaced on a piece-meal basis.

d. type of asbestos insulation product

It may be of relevance to know whether the claimant worked with, or was likely to have worked with, different kinds of asbestos insulation product. Products that were cut; that were sprayed on as dry fibre; or which required mixing from dry powder form with water to make cement - were each more likely to cause exposure to airborne fibre than, say, uncut sheets or boards. Likewise, asbestos insulation made from an amphibole fibre had a greater causal potency than of the non-amphibole type.

e. exposure to asbestos fibre from other manufacturers

In assessing the probability that a particular claimant's illness was caused by exposure to Hardie-BI product, it would seem logical to know the worker's exposure over time to asbestos fibre from all sources. Logically, it would seem to be more difficult to infer the necessary causal role of Hardie-BI fibre in respect of a worker exposed to asbestos fibre from many different sources over a long period of time than in respect of a worker who was only ever exposed to fibre from Hardie-BI product. But, that statement itself is somewhat controversial in relation to 'indivisible' injuries.

f. nature of illness

In terms of the attribution of causal significance to Hardie-BI product in respect of a given worker's illness, the nature of that illness may be of importance. Bearing in mind Professor Henderson's opinion that, with the malignant forms of illness, all exposure (above background) is causative, exposure to asbestos of other origin is not necessarily so significant. However, for non-malignant forms of illness the same principle does not apply so that it is at least relevant in respect of those illnesses to evaluate the relative degrees of exposure to all product to form a view of causation (ie liability).

But even if liability can be assumed, the question of the degree of responsibility of the Hardie-BI partners for a worker's damage consequent upon an illness, vis-à-vis other contributors, may require an assessment of the relative amounts of exposure. Whether that is so for both divisible and indivisible illnesses remains a live issue.

g. interval between exposure and onset of illness

A necessary ingredient for finding a causal relationship between an identified (or inferred) exposure to Hardie-BI fibre and a worker's illness, is the existence of a minimum gap in time before onset of the illness. An onset that occurs too close to the posited exposure event will not be attributed to that event because of the known latency period between exposure and the manifestation of illness in relation to different illnesses. Professor Henderson has examined each claimant against that criterion.[62]

[159]

Asbestos products that appear not to have been supplied by the Hardie-BI partnership but only by other manufacturers were webbing tape, rope lagging and limpet.

Both in respect of materials used in the construction phase of the two power stations built during the Hardie-BI partnership period and the maintenance phases for all of the power stations it is likely that Hardie-BI ATI was the dominant insulating material that was used. That is especially so in respect of pipes where blocks and sections made from calcium silicate foundation became the favoured form of insulation as time progressed.

The power stations constructed during the Hardie-BI period (Hazelwood and Yallourn W) were significantly more likely to contain large amounts of Hardie-BI ATI than those power stations built prior to the period (Yallourn and Morwell). That probability follows because, with respect to the newly constructed plants, the entire plant needed to be insulated from the outset and, by the mid-1960s, Hardie-BI's K-Lite and High Temp products were more and more being used in preference to other forms of insulation. However, it is also apparent that some of the materials used in the early phases of stages 1, 2 and possibly even 3 of the construction of the Hazelwood Power Station were sourced from James Hardie before the partnership period.

The insulation of large, flat surfaces around the boilers often used millboard product, or at least included it within the suite of other insulation materials. As millboard was made by a number of manufacturers such materials may well have been made by Hardie-BI or other manufacturers.

Before the commencement of the partnership period, James Hardie was also a significant supplier of ATI to the power station industry. Therefore, there was a strong degree of likelihood that its ATI was used prominently in the construction of power stations built before the 1960s - including Yallourn and Morwell. But it was equally likely that the replacement of ATI during the maintenance and repair for those sites built before the 1960s also featured prominent use of James Hardie ATI.

Because of the increasing preference for the use of the calcium silicate product, K-Lite (manufactured by the Hardie-BI partnership), over the older 85% magnesia product as time progressed from the mid-1960s through to the 1970s, the incidence of the use of Hardie-BI product in construction and maintenance probably increased relative to the use of products of other manufacturers.

The likelihood that Hardie-BI product was used in very substantial amounts in the construction of the Hazelwood Power Station is greater than in respect of the construction of Yallourn West. That is so because the evidence suggests that, at least in respect of the boilers, the head contractor at Hazelwood (Babcock and Wilcox) used Hardie-BI Super High Temp product almost exclusively. Babcock and Wilcox were not the head contractors at Yallourn West. Further, Hardie-BI's own partnership records indicate that while sales of its product were still being made to Yallourn West in the early 1970s, those sales were below what was expected.

From the typical profile given of the various trades represented amongst the eight sub-group claimants it appears that, in very general terms, the risk of the worker being exposed to asbestos fibre was in this order (from greatest to least): laggers; riggers; cleaners; fitters; instrument makers; electricians and tremors.

[178]

In my opinion the whole of the evidence establishes the probability that Mr Benjamin was exposed to some asbestos dust released from Hardie-BI product while working as an instrument maker at Yallourn West and Hazelwood Power Stations. An inference can be drawn from all of the evidence that he would at least have been exposed as a bystander while pre-formed Hardie-BI lagging was removed and replaced on pipes to enable him to access instruments. At least some of the lagging to which he was exposed, in particular the lagging that was being removed to enable access to instruments, would as a matter of probability have been Hardie-BI product supplied before December 1971, especially at Hazelwood.

Given that his first six months (to July 1971) at Yallourn power station was in training, it is likely that the vast majority of any of his exposure to ATI was after December 1971, although there may have been some exposure before that date. But having regard to the relatively short duration and that he was probably only exposed (if at all) as a bystander, I could not be satisfied as a matter of probability that he was exposed, specifically, to Hardie-BI asbestos before December 1971 although it seems likely he would have had some light to moderate exposure to ATI in his training and early work as an apprentice. It remains possible that in his second stint of work at Yallourn power station for five months in 1972/1973 he may have been exposed to Hardie-BI product that had been supplied before 31 December 1971, but I could not draw any such inference as a matter of probability.

I also find it is probable that he was exposed to some ATI product of other manufacturers, not only at the three power stations but also in his later employments at other locations and with other employers. Overall, it is very difficult to estimate what relative degree of exposure he may have had to Hardie-BI and non-Hardie-BI asbestos other than to say that each was likely to have been of some significant degree.[76]

[215]

We respectfully agree with Allsop P.

The rule that a plaintiff must establish as a necessary condition of recovery that he or she would not have suffered loss but for the defendant's actionable misconduct is deeply rooted in the policy of the common law that one person should not be liable for the loss suffered by another unless the plaintiff can establish that the defendant's actionable conduct caused the plaintiff's loss. It is not open to this Court to decide that we should no longer adhere to this rule and that a different and 'better' rule should henceforth be applied. This Court must proceed on the footing that for Mr Peterson to show that the consumption of Vioxx materially contributed to his MI, in the sense relevant in Australian law, he is obliged to show that his consumption of Vioxx was a necessary condition for the occurrence of the heart attack on 8 December 2003. To say that the consumption of Vioxx was, for example, 'in the mix' of possible causes is not enough in this regard. As Beazley JA said in Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307 at 339, the onus of proof of causation 'is not discharged by establishing that a particular matter cannot be excluded as a cause of the injury'.

The issue in Mr Johnstone's case is whether his exposure to asbestos was a necessary condition of his lung cancer. In other words, the question was: has it been proven as a matter of probability that, but for his exposure to asbestos, he would not have developed lung cancer?

Mr Johnstone was a long standing but light cigarette smoker all his life until the diagnosis of his illness. There is no doubt that cigarette smoking is recognised as a causal factor in the development of lung cancer.

The debate before me centred on whether, to establish the probable causal role of asbestos inhalation in lung cancer, it was necessary to show that the lung cancer patient also had asbestosis or only that he or she had inhaled enough asbestos to cause asbestosis. There was also a factual issue as to whether Mr Johnstone did have asbestosis, and failing that, whether he had inhaled sufficient amount of asbestos fibre that could cause asbestosis.

Professor Henderson summarised what he considered to be the state of medical knowledge in a series of bullet points in his written report:

[216]

For malignant mesothelioma, the sole identifiable cause in most cases is asbestos fibre inhalation - especially amphibole asbestos. Only rare cases of mesothelioma can be related to other factors such as ionising radiation (in my experience, most mesotheliomas in those with a background of radiation have also had identified exposure(s) to asbestos), or to an underlying innate susceptibility factor such as the BAPI Tumour Predisposition Syndrome. Tobacco smoking is not a causal factor for mesothelioma induction. In contrast, lung cancer comprises a heterogeneous group of cancers with multifactorial causes, which include cigarette smoke (the most potent known factor - please note that this report does not discuss the issue of passive smoking - no such information is available for any of the cases), asbestos, radiation (such as radon gas), certain heavy metals (such as hexavalent chromium and arsenic), toxic fumes, air pollution, innate susceptibility factors and so forth.
There are no significant clinical, radiological or pathological differences between lung cancers found in cigarette smokers versus asbestos-exposed individuals, versus those for whom neither factor is identifiable. That is, there are no identifiable differences per se for a particular lung cancer that would allow one to assign asbestos causation, or some other cause.
Most lung cancers among asbestos workers occur in those who are (or were) cigarette smokers.
There is a known synergistic (multiplicative or submultiplicative) interaction between cigarette smoke and asbestos fibre inhalation, for the causation of lung cancer. That is, the joint effect is greater than the sum of the individual carcinogenic effects, and this interactive effect cannot be assigned back to the individual effect of each (i.e., to cigarette smoke; asbestos).
Because of this interplay between causal factors, assessment of causation of lung cancer is a more complex exercise than assignment of asbestos causation for a malignant mesothelioma.
Assessment of causation of lung cancer among workers with asbestos exposure is, therefore, a probabilistic exercise.
The presence of asbestosis has been used in the past as a marker for substantial asbestos exposure and has been used as a marker for a significant causal contribution from asbestos exposure for lung cancer causation (and still is, when it is diagnosable as such).
Some authorities have invoked asbestosis as the only 'consistent' indicator for lung cancer causation by asbestos (e.g., Cagle, 2002).
A focus on asbestosis as the sole and an obligate identifier for lung cancer causation is beset with problems and does not accord with the prevailing scientific literature ...[References to literature omitted]
A requirement for asbestosis cannot readily explain the synergy between cigarette smoke and asbestos, and the dose-response relationship between asbestos and lung cancer.
Asbestos fibres themselves are carcinogenic (e.g., for causation of mesothelioma); it seems inconsistent to argue that they are entirely non-carcinogenic for lung cancer causation, and that it is the interstitial fibrosis of asbestosis that is the causal agent.
Current majority opinion favours the class, character and magnitude of the asbestos exposure itself as the causal factor, with no requirement for asbestosis.
In most workplaces in Australia (unlike Germany and Sweden). There were no systematic serial measurements of airborne asbestos fibres to set forth numerical estimates of cumulative exposure expressed as fibres/mL-years for the particular work place, although one can estimate from the work history and type(s) of work carried out, that the cumulative exposure would have been, say, >25 fibre-years (or, on the other hand, that the exposure would have trivial and inconsistent, with exposure incompatible with the exposures necessary to cause asbestosis in some cases).
For many if not most cases of asbestos-associated lung cancer, no lung tissue is available for a formal assay of Abs and/or uncoated asbestos fibres (UCAFs).
Therefore, I place considerable emphasis on work history for assessment of asbestos causation of lung cancer - was the exposure of a class, character and magnitude that it would be consistent with diagnosis of asbestosis, either for the lung cancer patient (whether or not there was such a diagnosis) or for other workers carrying out similar work in similar work places, at similar times and for similar durations of time?

[217]

Professor Henderson was asked to express his view on the balance of probabilities as to whether any exposure to asbestos during the Hardie-BI period had made a significant causal contribution to the development of Mr Johnstone's lung cancer. He answered as follows:

Yes, for causation of Mr Johnstone's non-small cell of lung, from his exposure at the YPS within the Hardie-BI period - i.e., in the years 1973 to 1974 (for a period of ~ 16 months) - 'on the balance of probabilities'. My opinion is based on his occupational work/exposure history, Dr Kilpatrick's assessment of his cumulative (total) exposure as >25 fibre-years and the clinical-radiological evidence of interstitial fibrosis (asbestosis). Although the Hardie-BI YPS exposure lasted for ~ 16 months, it would have made a more than trivial causal contribution to the development of his lung carcinoma and to the development and severity of any asbestosis, as well as the development of pleural plaque tissue.

Professor Fox did not accept that the true test for the causal role of asbestos in lung cancer was that it was sufficient only to show enough exposure to cause asbestosis. He considered that the view accepted by the wider medical community was that a diagnosis of asbestosis was necessary to make the causal role of asbestos a probability. He also disagreed with Professor Henderson that the combined effect of smoking and asbestos inhalation was synergistic (that is multiplicative) - he believed it was only additive. In any event, he doubted that Mr Johnstone had achieved the exposure criteria of 25 fibre mls per year, known as the Helsinki criteria.

Professor Henderson's reference to Dr Kilpatrick's assessment of a cumulative exposure of more than 25 fibre mls per year was a reference to a report to which Professor Fox had not had access at the time of writing his own report.

Professor Henderson believed that Mr Johnstone did in fact exhibit sufficient signs of asbestosis for it to be concluded that he had that condition. For his part, Professor Fox thought that the radiological evidence of asbestosis was inconclusive and had recommended further investigation.

This issue seems to have been satisfactorily resolved in favour of Professor Henderson's view. Mr Johnstone subsequently died and an autopsy report showed the presence of asbestos bodies in his lungs. When that report was shown to Professor Henderson he concluded that there was a 'persuasive diagnosis of asbestosis' because the presence of asbestos bodies represented a good delineator between asbestosis, on the one hand, and a non-asbestosis form of interstitial lung disease, on the other. Professor Henderson was not challenged on that view in cross-examination. Although he could not say with certainty that Mr Johnstone would not have developed lung cancer without being exposed to asbestos, Professor Henderson believed it was more likely than not that asbestos had contributed significantly to the lung disease.

In my opinion, I can and should accept that the evidence establishes that Mr Johnstone's exposure to asbestos fibre in general played a non-trivial causal role in the development of his lung cancer. Professor Henderson was not challenged in his view that there was a multiplicative relationship between the combined agents of tobacco smoke and asbestos fibre in causing lung cancer. When asked whether he could assign the proportional role between tobacco smoke and asbestos Professor Henderson thought he could only say that the asbestos had made a 'significant' - 'more than trivial ... more than negligible' causal contribution to the lung cancer disease. In his written report he said:

His cigarette smoking would have also had a substantial causal effect. His lung cancer can be attributed on probabilistic grounds to the combined synergistic effects of his tobacco smoking and his asbestos exposure by way of causal co-action, with an interactive effect which by definition is not separable/fractionable into the individual effects of tobacco smoke and asbestos.[92]

[268]

I reject James Hardie's interpretation of what Dean J said in Allman about sub-s (4) being of 'universal application', namely that it was confined only to contribution actions by a wrongdoer who had been served with a writ. A close reading of his Honour's judgment shows that the third party argued that the limitation section was 'of general application and provided a period of limitation in all cases where a defendant sought contribution from a third party pursuant to the Act'. The defendant had argued that the sub-section was not intended to provide a general limitation of time applicable to all claims, but only for those cases affected by a special statutory provision as to notice before action or the time in which a defendant might be sued.

Although not on all fours with the argument raised by James Hardie in this case, the defendant's argument in Allman was similar in concept. The defendant wanted to confine the sub-section's application to only that subset of cases that featured a constraint of the kind expressly mentioned in the sub-section (ie being affected by another potential time limit). Dean J rejected that construction. In a similar way, in this case, James Hardie wants to confine the operation of sub-s (4) to only that subset of cases that feature another condition appearing in the sub-section, namely, that a writ has been served on the person seeking contribution.

But, when his Honour referred to 'a new and universal rule', he was, in my view, signalling that this rule was to cover all instances of contribution claims brought under the enactment. There is simply no room left in the language used by his Honour for exception or excision.

In my view, his Honour was (with respect) correct in this regard. This was a new right, and Parliament was cautious about its extension into unknown territory. Rather than support its view, the extrinsic materials to which James Hardie referred tends to support the opposite view. As revealed by those materials, the dominant focus at that point in the evolution of tortfeasors' rights of contribution was the right of a defendant after being served by an injured party with a writ.

...

In State Electricity Commission of Victoria v Fooks Tadgell J (with whom Brooking and Smith JJ agreed) appeared to construe the reference to the writ in s 24(4)(ii) as being a reference to the writ served by the injured party claiming the damage the liability to pay compensation for which gave rise to the entitlement to recover contribution. Although s 24(4)(a)(ii) used slightly different language to its pre-1972 antecedent, the construction given to it by the Full Court in 1994 tends to corroborate the view that the cognate expression used in the pre-1972 provision also meant a writ that was initiated by the injured party. In that respect I agree with the construction given to it by James Hardie.

But, the Full Court's construction of the post-1972 provision is consistent with the view that the subsection is a limitation provision to cover all eventualities, of which a tortfeasor being served with a writ by the injured party is just one. As it was after 1972, so it was before 1972. The introduction by the 1972 amendment of additional events that could set off the limitation period is not to be taken as converting a limitation provision of narrow application into one of universal application. Rather, it was an amendment to cure various lacunae left by the original provision.

James Hardie attempted to support its position by arguing that s 24 is neatly divided into three discrete parts: that is, s 24(1)(c) concerns entitlement; s 24(2) concerns apportionment; and s 24(4) deals only with limitation. It argued that it is wrong to construe the operation of the limitation provision in a way that affects substantive entitlement. Accepting that s 24(4) operated only if a writ in the original action was served on the party pursuing contribution, it argued that those who had not been served with the writ must therefore have their time limit governed by another statute. Alternatively, there is no applicable limitation provision.

I was initially attracted to James Hardie's argument. But two things can be said against it. First, the requirement of service of a writ is not expressed as a condition for the ascertainment of the entitling liability referred to in sub-s (1)(c): rather, it is a procedural prerequisite for the ability to commence the action. Whilst it might have a practical effect of limiting the entitlement, it is not itself a qualification of the entitling words in sub-s (1)(c).

But having that practical effect is not necessarily to be regarded as inconsistent with the contemporary conception of the right, or the circumstances in which it was assumed to operate. Interpretations of the legislation by 1958 did not categorically accept that the tortfeasor pursuing the contribution could be 'liable' other than by judgment. Or, to the extent settlement was contemplated to be a sufficient basis for liability, it was not clearly accepted that such a basis could be founded on a settlement without action. In Bitumen and Oil in 1955, the High Court did not find it necessary to decide whether a tortfeasor who had settled could be 'liable' so as to seek contribution. In Brambles Constructions Pty Ltd v Helmers in 1966, Windeyer J said that liability was 'ordinarily [ascertained] by judgment, perhaps in some cases in some other way'. Only in 1996, in Thompson v Australian Capital Television Pty Ltd, was it finally acknowledged in the High Court, following Australian State and Territory decisions, that liability of the first tortfeasor included a liability ascertained upon a settlement, whether or not reflected in a consent judgment.

In short, the conclusion that was ultimately reached in Australia that the liability spoken of in sub-s (1)(c) need not be a liability by judgment was not self-evident in 1949 or even in 1958. Having that knowledge assists in explaining what otherwise seems like a clear anomaly today. It makes reasonable a construction of sub-s (4) that does not allow for an effective right of contribution for a wrongdoer not served with a writ in the original action brought by the injured party.

Finally, any so-called injustice of this outcome is not as great as may be supposed and ought not to be used as an imperative for searching for an alternative. A would-be seeker of contribution could, before agreeing to pay any contribution that gave rise to the right to claim it from another, have insisted upon being served with a writ, in which case that person would have a year to commence a contribution claim.[112]

[394]

Having made the choice that it made, any delay in informing CSR of the existence of the Reid claim, the proposal to settle it and the fact of settling it, and then joining it to the proceeding was apt to prejudice CSR's ability to undertake its own investigations of the circumstances of the injury.

A number of circumstances could combine to give rise to that prejudice if there should be further, unreasonable delay, namely: the long latency period between exposure and illness created a situation of urgency for the preservation of whatever relevant factual material might still exist; the nature of the condition meant that the time frame within which to obtain relevant medical and other information directly from the claimant was limited; the 'control' over such other information that could be obtained was, in substance, exercised by James Hardie under its GSA entitlements; and the choice James Hardie made as to the omnibus form of the litigation extended the delay between issue and trial.

Once a claim was settled by the SECV attracting the operation of the GSAs, James Hardie ought to have acted swiftly to make its payment and join the claim to the proceeding. In this particular case the cumulative delays of nearly six years between the SECV settlement and the JHC payment and then the JHC payment to the commencement of this proceeding has added an unacceptable and unreasonable additional period of time before this matter has come to trial. All of the relevant time frames in this case are longer than those relating to Mr Alexander, including those over which I presume James Hardie had a degree of control. The length of the delays of themselves call for some explanation. But, without explanation, nearly six years elapsed from settlement and nearly 3½ years elapsed from contribution before the claim was brought. During that time it may reasonably be inferred that some evidence which might have been gathered to assist CSR in defending the claim would have either been lost or made less readily accessible.

There is an air of artificiality in James Hardie's insistence that CSR should identify with greater specificity the evidence that was lost, or the precise way in which it was prejudiced, or the actual period of 'excessive' delay. These requirements call for CSR to identify the very things it could not know by reason of the position in which it was placed by the long latency period of the disease and the choices James Hardie made in the arrangement under which it settled claims.[184]

[418]

(a) the judge did not err in admitting the asbestos exposure histories contained in medical reports relating to individual claimants. Accordingly, CSR's grounds 1 and 2 fail;

(b) the judge did not err in drawing the inferences he drew relating to the claimants whom he found were exposed to Hardie-BI asbestos product. Nor did he err in concluding that those exposures were a cause of the injuries suffered by those claimants. Accordingly, CSR's grounds 3 and 4 fail;

(c) the judge did not err in concluding that the claimants Mr Johnstone, Mr Benjamin, Mr Alexander, Mr Kracht, Mr McGuire and Mr Preston were exposed to Hardie-BI product and that that exposure was a cause of their injuries. Accordingly, CSR's grounds 6 to 10 fail - except ground 8 (relating to Alexander) to a limited extent. In respect of the Alexander claim, the judge erred in finding that there were different causal potencies for different types of asbestos in respect of asbestosis. The correction of that error means that the amount of contribution awarded by the judge in respect of Mr Alexander ($35,000) should be reduced to $12,500;

(d) the judge did not err when he concluded that the equitable right of contribution was not subsumed within or overtaken by the statutory remedy provided by s 24 of the Wrongs Act. Accordingly, CSR's ground 5 fails. However the judge erred when he concluded that claims for equitable contribution were only available where no statutory claim for contribution was available. Accordingly, James Hardie's cross-appeal ground 3 succeeds and James Hardie has a claim for equitable contribution in respect of every claimant who was relevantly exposed to Hardie-BI product and who suffered injury as a result;

(e) the judge did not err in his conclusion that the defence of laches is available in claims for equitable contribution notwithstanding the existence of a statutory limitation period applied by analogy. Accordingly, James Hardie's cross-appeal ground 1 fails; and

(f) the judge erred in concluding that the equitable contribution claims in respect of Mr Reid and Mr Preston were defeated by laches. In those cases, the defence of laches was not made out. Accordingly, James Hardie's cross-appeal ground 2 succeeds.

At a glance

Court

Decision date

Before

Source

Judgment (517 paragraphs)

Parties

Legislation Cited (5)

Cases Cited (18)